Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Enterobacter Infections

  • Author: Susan L Fraser, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Oct 07, 2015
 

Practice Essentials

Enterobacter infections can include bacteremia, lower respiratory tract infections, skin and soft-tissue infections, urinary tract infections (UTIs), endocarditis, intra-abdominal infections, septic arthritis, osteomyelitis, CNS infections, and ophthalmic infections. Enterobacter infections can necessitate prolonged hospitalization, multiple and varied imaging studies and laboratory tests, various surgical and nonsurgical procedures, and powerful and expensive antimicrobial agents.

Essential update: CDC expands guidelines for carbapenem-resistant Enterobacteriaceae

The Centers for Disease Control and Prevention (CDC) has expanded its guidelines for preventing the spread of carbapenem-resistant Enterobacteriaceae (CRE). Noting that most cases of CRE found in the United States have been isolated from patients who received overnight treatment in medical facilities outside the country, the new recommendations are as follows[1, 2] :

  • When a CRE is found in a patient who within the previous 6 months had stayed overnight in a non-US health-care facility, the isolate should undergo confirmatory susceptibility testing and the carbapenem resistance mechanism should be determined
  • Rectal screening cultures should be ordered for any patient admitted to a health-care facility in the United States after being hospitalized within the previous 6 months in another country; such patients should be placed on contact precautions until the results of the screenings are available.

Signs and symptoms

Enterobacter infections do not have a clinical presentation that is specific enough to differentiate them from other acute bacterial infections.

Bacteremia

Signs of Enterobacter bacteremia include the following:

  • Physical examination findings consistent with systemic inflammatory response syndrome (SIRS): Including heart rate that exceeds 90 bpm, a respiratory rate greater than 20, and a temperature above 38°C or below 36°C
  • Fever: Occurring in more than 80% of children and adults with Enterobacter bacteremia
  • Hypotension and shock: Occur in as many as one third of cases
  • Septic shock: Manifested as disseminated intravascular coagulation, jaundice, acute respiratory distress syndrome, and other complications of organ failure
  • Purpura fulminans and hemorrhagic bullae
  • Ecthyma gangrenosum
  • Cyanosis and mottling: Frequently reported in children with Enterobacter bacteremia

Lower respiratory tract infections

Enterobacter lower respiratory tract infections can manifest identically to those caused by Streptococcus pneumoniae or other organisms. The physical examination findings may include the following:

  • Apprehension
  • High fever or hypothermia
  • Tachycardia
  • Hypoxemia
  • Tachypnea
  • Cyanosis

Patients with pulmonary consolidation may present with crackling sounds, dullness to percussion, tubular breath sounds, and egophony. Pleural effusion may manifest as dullness to percussion and decreased breath sounds.

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies

Studies for the evaluation of Enterobacter infections include the following:

  • Complete blood count
  • Creatinine level
  • Electrolyte evaluation
  • Fluid analysis, such as cells and differential, proteins, glucose, and, in some cases, pH, lactate dehydrogenase, and amylase; required for pleural, articular, pericardial, peritoneal, and cerebrospinal fluids
  • Urine analysis: Always indicated for urinary tract infections (UTIs)

Factors in the microbiologic diagnosis and assessment of Enterobacter infection include the following:

  • The most important test to document Enterobacter infections is culture; when the patient presents with signs of systemic inflammation (eg, fever, tachycardia, tachypnea) with or without shock (eg, hypotension, decreased urinary output), blood cultures are mandatory
  • Direct Gram staining of the specimen is also useful, because it allows rapid diagnosis of an infection caused by gram-negative bacilli and helps in the selection of antibiotics with known activity against most of these bacteria
  • In the laboratory, growth of Enterobacter isolates is expected to be detectable in 24 hours or less; Enterobacter species grow rapidly on selective (ie, MacConkey) and nonselective (ie, sheep blood) agars

Imaging studies

Studies used in the investigation and management of Enterobacter infections include the following:

  • Chest infections: Serial chest radiography, chest ultrasonography, and computed tomography (CT) scanning
  • Intra-abdominal infections: CT scanning and ultrasonography
  • Endocarditis and intravascular infections: Echocardiography (preferably transesophageal) and nuclear indium scanning
  • UTIs: Renal ultrasonography; occasionally, CT scanning and pyelography
  • Central nervous system (CNS) and ophthalmic infections: CT scanning and/or magnetic resonance imaging (MRI)
  • Bone and joint infections: Plain radiography, CT scanning and/or MRI studies, nuclear medicine studies

New technologies such as positron emission tomography (PET) scanning may be indicated in very selective cases, particularly for differentiation of neoplasia and infection.

See Workup for more detail.

Management

Antimicrobial therapy is indicated in virtually all Enterobacter infections. With few exceptions, the major classes of antibiotics used to manage infections with these bacteria include the following:

  • Beta-lactams: Carbapenems are the most reliable beta-lactam drugs for the treatment of severe Enterobacter infections; fourth-generation cephalosporins are a distant second choice
  • Aminoglycosides: Aminoglycoside resistance is relatively common and varies widely among centers
  • Fluoroquinolones: Resistance to fluoroquinolones is relatively rare but may be high in some parts of the world
  • Trimethoprim-sulfamethoxazole (TMP-SMZ): Resistance to TMP-SMZ is more common

See Treatment and Medication for more detail.

Next

Background

Enterobacter species, particularly Enterobacter cloacae and Enterobacter aerogenes, are important nosocomial pathogens responsible for various infections, including bacteremia, lower respiratory tract infections, skin and soft-tissue infections, urinary tract infections (UTIs), endocarditis, intra-abdominal infections, septic arthritis, osteomyelitis, CNS, and ophthalmic infections. Enterobacter species can also cause various community-acquired infections, including UTIs, skin and soft-tissue infections, and wound infections, among others.

Risk factors for nosocomial Enterobacter infections include hospitalization of greater than 2 weeks, invasive procedures in the past 72 hours, treatment with antibiotics in the past 30 days, and the presence of a central venous catheter. Specific risk factors for infection with nosocomial multidrug-resistant strains of Enterobacter species include the recent use of broad-spectrum cephalosporins or aminoglycosides and ICU care.

These "ICU bugs" cause significant morbidity and mortality, and infection management is complicated by resistance to multiple antibiotics. Enterobacter species possess inducible beta-lactamases, which are undetectable in vitro but are responsible for resistance during treatment. Physicians treating patients with Enterobacter infections are advised to avoid certain antibiotics, particularly third-generation cephalosporins, because resistant mutants can quickly appear. The crucial first step is appropriate identification of the bacteria. Antibiograms must be interpreted with respect to the different resistance mechanisms and their respective frequency, as is reported for Enterobacter species, even if routine in vitro antibiotic susceptibility testing has not identified resistance.

Previous
Next

Pathophysiology

Enterobacter species rarely cause disease in healthy individuals. This opportunistic pathogen, similar to other members of the Enterobacteriaceae family, possesses an endotoxin known to play a major role in the pathophysiology of sepsis and its complications.

Although community-acquired Enterobacter infections are occasionally reported, nosocomial Enterobacter infections are, by far, most common. Patients most susceptible to Enterobacter infections are those who stay in the hospital, especially the ICU, for prolonged periods. Other major risk factors of Enterobacter infection include prior use of antimicrobial agents, concomitant malignancy (especially hemopoietic and solid-organ malignancies), hepatobiliary disease, ulcers of the upper gastrointestinal tract, use of foreign devices such as intravenous catheters, and serious underlying conditions such as burns, mechanical ventilation, and immunosuppression.

The source of infection may be endogenous (via colonization of the skin, gastrointestinal tract, or urinary tract) or exogenous, resulting from the ubiquitous nature of Enterobacter species. Multiple reports have incriminated the hands of personnel, endoscopes, blood products, devices for monitoring intra-arterial pressure, and stethoscopes as sources of infection. Outbreaks have been traced to various common sources: total parenteral nutrition solutions, isotonic saline solutions, albumin, digital thermometers, and dialysis equipment.

Enterobacter species contain a subpopulation of organisms that produce a beta-lactamase at low-levels. Once exposed to broad-spectrum cephalosporins, the subpopulation of beta-lactamase–producing organisms predominate. Thus, an Enterobacter infection that appears sensitive to cephalosporins at diagnosis may quickly develop into a resistant infection during therapy. Carbapenems and cefepime have a more stable beta-lactam ring against the lactamase produced by resistant strains of Enterobacter.

Previous
Next

Epidemiology

Frequency

United States

National surveillance programs continually demonstrate that Enterobacter species remain a significant source of morbidity and mortality in hospitalized patients.

In the Surveillance and Control of Pathogens of Epidemiological Importance [SCOPE] project, 24,179 nosocomial bloodstream infections from 1995-2002 were analyzed. Enterobacter species were the second-most-common gram-negative organism behind Pseudomonas aeruginosa; however, both bacteria were reported to each represent 4.7% of bloodstream infections in ICU settings. Enterobacter species represent 3.1% of bloodstream infections in non-ICU wards. Of nearly 75,000 gram-negative organisms collected from ICU patients in the United States between 1993 and 2004, Enterobacter species comprised 13.5% of the isolates. Multidrug resistance increased over time, especially in infections caused by E cloacae.[3]

The National Healthcare Safety Network (NHSN) reported on healthcare-associated infections (HAI) between 2006 and 2007. They found Enterobacter species to be the eighth most common cause of HAI (5% of all infections) and the fourth most common gram-negative cause of HAIs.[4]

Previous reports from the National Nosocomial Infections Surveillance System (NNIS) demonstrated that Enterobacter species caused 11.2% of pneumonia cases in all types of ICUs, ranking third after Staphylococcus aureus (18.1%) and P aeruginosa (17%). The corresponding rates among patients in pediatric ICUs were 9.8% for pneumonia, 6.8% for bloodstream infections, and 9.5% for UTIs.[5, 6, 7]

Enterobacter species were also among the most frequent pathogens involved in surgical-site infections, as reported in the NNIS report from October 1986 to April 1997. The isolation rate was 9.5% (with enterococci, coagulase-negative staphylococci, S aureus, and P aeruginosa rates being 15.3%, 12.6%, 11.2%, and 10.3%, respectively).

Data on antibiotic resistance are available from the Intensive Care Antimicrobial Resistance Epidemiology (ICARE) surveillance report. The rates of Enterobacter resistance to third-generation cephalosporins were 25.3% in ICUs, 22.3% among non-ICU inpatients, 10.1% among ambulatory patients, and as high as 36.2% in pediatric ICUs.[8]

International

Enterobacter species have a global presence in both adult and neonatal ICUs. Surveillance data and outbreak case reports from North and South America, Europe, and Asia indicate that these bacteria represent an important opportunistic pathogen among neonates and debilitated patients in ICUs.

The prevalence of Enterobacter resistance to beta-lactam antibiotics, aminoglycosides, trimethoprim-sulfamethoxazole (TMP-SMZ), and quinolones seems to be higher in certain European countries and Israel than in the United States and Canada. Higher rates of Enterobacter resistance to fluoroquinolones and to beta-lactam and cephalosporin antibiotics due to the production of extended-spectrum beta-lactamases have been reported in South America and the Asian and Pacific regions.[9, 10]

Mortality/Morbidity

Enterobacter infections cause considerable mortality and morbidity rates.

Enterobacter species can cause disease in virtually any body compartment. They are responsible for frequent and severe nosocomial infections that require prolonged hospitalization, multiple and varied imaging studies and laboratory tests, various surgical and nonsurgical procedures, and powerful and expensive antimicrobial agents. Most importantly, Enterobacter infections that do not directly causing death cause considerable suffering in many patients, most of whom are already afflicted with chronic diseases.

In patients with Enterobacter bacteremia, the most important factor in determining the risk of mortality is the severity of the underlying disease. Higher 30-day mortality rates were noted in patients presenting with septic shock and increasing Acute Physiology and Chronic Health Evaluation II scores. Other factors implicated, independently or by association, in the outcome of Enterobacter bacteremia include thrombocytopenia, hemorrhage, a concurrent pulmonary focus of infection, renal insufficiency, admission in an ICU, prolonged hospitalization, prior surgery, intravascular and/or urinary catheters, immunosuppressive therapy, neutropenia, antibiotic resistance, and inappropriate antimicrobial therapy.

Recent studies have demonstrated that empirical aminoglycoside use and appropriate initial antibiotic therapy were associated with lower mortality rates, whereas vasopressor use, ICU care, and acute renal failure were associated with higher mortality rates. Independent risk factors for mortality included cephalosporin resistance, trimethoprim-sulfamethoxazole resistance, mechanical ventilation, and nosocomial infection.[11, 12]

Crude mortality rates associated with Enterobacter infections range from 15-87%, but most reported rates range from 20-46%. Attributable mortality rates are reported to range from 6-40%.

E cloacae infection is associated with the highest mortality rate of all Enterobacter infections.

Bacteremia with cephalosporin-resistant Enterobacter species is associated with a 30-day mortality rate that significantly exceeds that of infections with susceptible strains (33.7% vs 18.6%).

Mortality rates associated with Enterobacter pneumonia are higher than those of pneumonia due to many other gram-negative bacilli. These rates range from 14-71%. As with bacteremia, the severity of the underlying disease is the major factor that predicts outcome. Other factors that indicate an unfavorable outcome include the extent of the disease as seen on chest radiographs, corticosteroid therapy, isolation of multiple pathogens from lower respiratory tract secretions, and, possibly, treatment with a single antibiotic.

A review of 17 cases of Enterobacter endocarditis reported an overall mortality rate of 44.4%.

Race

Enterobacter infections have no reported or presumed racial predilection.

Sex

The male-to-female ratio of Enterobacter bacteremia is 1.3-2.5:1. This male predominance is also reported in the pediatric population.

Age

Enterobacter infections are most common in neonates and in elderly individuals, reflecting the increased prevalence of severe underlying diseases at these age extremes. In the pediatric ICU setting, an age younger than 2.5 years is a risk factor for colonization.

Enterobacter sakazakii, now known as Cronobacter sakazakii, has been reported as a cause of sepsis and meningitis, complicated by ventriculitis, brain abscess, cerebral infarction, and cyst formation.[13] This clinical pattern appears to be specific to C sakazakii in neonates and infants infected with this bacterium. C sakazakii has also been associated with many outbreaks due to contaminated powdered formula for infants.[14, 15]

A taxonomic reclassification of the neonatal pathogen E sakazakii within a new genus " Cronobacter " within the Enterobacteriaceae was proposed in 2007.[16]

Previous
 
 
Contributor Information and Disclosures
Author

Susan L Fraser, MD Chief, Infectious Diseases Service, Fort Belvoir Community Hospital; Chairman, Infection Control Committee; Associate Professor of Medicine, Uniformed Services University of the Health Sciences

Susan L Fraser, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Armed Forces Infectious Diseases Society

Disclosure: Nothing to disclose.

Coauthor(s)

Christian P Sinave, MD Associate Professor, Department of Medical Microbiology and Infectious Diseases, University of Sherbrooke Faculty of Medicine, Canada

Christian P Sinave, MD is a member of the following medical societies: American Society for Microbiology, Association of Medical Microbiology and Infectious Disease Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Joseph F John, Jr, MD, FACP, FIDSA, FSHEA Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina College of Medicine; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center

Joseph F John, Jr, MD, FACP, FIDSA, FSHEA is a member of the following medical societies: Charleston County Medical Association, Infectious Diseases Society of America, South Carolina Infectious Diseases Society

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Maria D Mileno, MD Associate Professor of Medicine, Division of Infectious Diseases, The Warren Alpert Medical School of Brown University

Maria D Mileno, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine, Sigma Xi

Disclosure: Nothing to disclose.

Acknowledgements

Michael Arnett, MD Resident Physician, Department of Medicine, Tripler Army Medical Center

Disclosure: Nothing to disclose.

References
  1. Fox S. Carbapenem-Resistant Enterobacteriaceae: New Precautions. Medscape Medical News. Feb 19 2013. [Full Text].

  2. Centers for Disease Control and Prevention. New Carbapenem-Resistant Enterobacteriaceae Warrant Additional Action by Healthcare Providers. CDC. Feb 14 2013. [Full Text].

  3. Lockhart SR, Abramson MA, Beekmann SE, et al. Antimicrobial resistance among Gram-negative bacilli causing infections in intensive care unit patients in the United States between 1993 and 2004. J Clin Microbiol. 2007 Oct. 45(10):3352-9. [Medline].

  4. Hidron AI, Edwards JR, Patel J, Horan TC, Sievert DM, Pollock DA. NHSN annual update: antimicrobial-resistant pathogens associated with healthcare-associated infections: annual summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006-2007. Infect Control Hosp Epidemiol. 2008 Nov. 29(11):996-1011. [Medline].

  5. National Nosocomial Infections Surveillance System. National Nosocomial Infections Surveillance (NNIS) report, data summary from October 1986-April 1997, issued May 1997. A report from the NNIS System. Am J Infect Control. 1997 Dec. 25(6):477-87. [Medline].

  6. National Nosocomial Infections Surveillance System. National Nosocomial Infections Surveillance (NNIS) System report, data summary from January 1990-May 1999, issued June 1999. Am J Infect Control. 1999 Dec. 27(6):520-32. [Medline].

  7. National Nosocomial Infections Surveillance System. National Nosocomial Infections Surveillance (NNIS) System Report, data summary from January 1992 through June 2004, issued October 2004. Am J Infect Control. 2004 Dec. 32(8):470-85. [Medline].

  8. National Nosocomial Infections Surveillance System. Intensive Care Antimicrobial Resistance Epidemiology (ICARE) Surveillance Report, data summary from January 1996 through December 1997: A report from the National Nosocomial Infections Surveillance (NNIS) System. Am J Infect Control. 1999 Jun. 27(3):279-84. [Medline].

  9. Rossi F, Baquero F, Hsueh PR, et al. In vitro susceptibilities of aerobic and facultatively anaerobic Gram-negative bacilli isolated from patients with intra-abdominal infections worldwide: 2004 results from SMART (Study for Monitoring Antimicrobial Resistance Trends). J Antimicrob Chemother. 2006 Jul. 58(1):205-10. [Medline].

  10. Chow JW, Satishchandran V, Snyder TA, et al. In vitro susceptibilities of aerobic and facultative gram-negative bacilli isolated from patients with intra-abdominal infections worldwide: the 2002 Study for Monitoring Antimicrobial Resistance Trends (SMART). Surg Infect (Larchmt). 2005 Winter. 6(4):439-48. [Medline].

  11. Deal EN, Micek ST, Ritchie DJ, et al. Predictors of in-hospital mortality for bloodstream infections caused by Enterobacter species or Citrobacter freundii. Pharmacotherapy. 2007 Feb. 27(2):191-9. [Medline].

  12. Ye Y, Li JB, Ye DQ, et al. Enterobacter bacteremia: Clinical features, risk factors for multiresistance and mortality in a Chinese University Hospital. Infection. 2006 Oct. 34(5):252-7. [Medline].

  13. Gallagher PG, Ball WS. Cerebral infarctions due to CNS infection with Enterobacter sakazakii. Pediatr Radiol. 1991. 21(2):135-6. [Medline].

  14. Drudy D, Mullane NR, Quinn T, et al. Enterobacter sakazakii: an emerging pathogen in powdered infant formula. Clin Infect Dis. 2006 Apr 1. 42(7):996-1002. [Medline].

  15. Yan QQ, Condell O, Power K, Butler F, Tall BD, Fanning S. Cronobacter species (formerly known as Enterobacter sakazakii) in powdered infant formula: a review of our current understanding of the biology of this bacterium. J Appl Microbiol. 2012 Mar 16. [Medline].

  16. Iversen C, Lehner A, Mullane N, Marugg J, Fanning S, Stephan R, et al. Identification of "Cronobacter" spp. (Enterobacter sakazakii). J Clin Microbiol. 2007 Nov. 45(11):3814-6. [Medline].

  17. Palmer DL, Kuritsky JN, Lapham SC, et al. Enterobacter mediastinitis following cardiac surgery. Infect Control. 1985 Mar. 6(3):115-9. [Medline].

  18. Tunkel AR, Fisch MJ, Schlein A, et al. Enterobacter endocarditis. Scand J Infect Dis. 1992. 24(2):233-40. [Medline].

  19. Durand ML, Calderwood SB, Weber DJ, et al. Acute bacterial meningitis in adults. A review of 493 episodes. N Engl J Med. 1993 Jan 7. 328(1):21-8. [Medline].

  20. Pathengay A, Trehan HS, Mathai A, et al. Enterobacter endophthalmitis: clinicomicrobiologic profile and outcomes. Retina. 2012 Mar. 32(3):558-62. [Medline].

  21. Maki DG, Weise CE, Sarafin HW. A semiquantitative culture method for identifying intravenous-catheter-related infection. N Engl J Med. 1977 Jun 9. 296(23):1305-9. [Medline].

  22. Paterson DL. Resistance in gram-negative bacteria: enterobacteriaceae. Am J Med. 2006 Jun. 119(6 Suppl 1):S20-8; discussion S62-70. [Medline].

  23. Ritchie DJ, Alexander BT, Finnegan PM. New antimicrobial agents for use in the intensive care unit. Infect Dis Clin North Am. 2009 Sep. 23(3):665-81. [Medline].

  24. Ratnam I, Franklin C, Spelman DW. In vitro activities of 'new' and 'conventional' antibiotics against multi-drug resistant Gram negative bacteria from patients in the intensive care unit. Pathology. 2007 Dec. 39(6):586-8. [Medline].

  25. Reinert RR, Low DE, Rossi F, et al. Antimicrobial susceptibility among organisms from the Asia/Pacific Rim, Europe and Latin and North America collected as part of TEST and the in vitro activity of tigecycline. J Antimicrob Chemother. 2007 Nov. 60(5):1018-29. [Medline].

  26. Halstead DC, Abid J, Dowzicky MJ. Antimicrobial susceptibility among Acinetobacter calcoaceticus-baumannii complex and Enterobacteriaceae collected as part of the Tigecycline Evaluation and Surveillance Trial. J Infect. 2007 Jul. 55(1):49-57. [Medline].

  27. DiPersio JR, Dowzicky MJ. Regional variations in multidrug resistance among Enterobacteriaceae in the USA and comparative activity of tigecycline, a new glycylcycline antimicrobial. Int J Antimicrob Agents. 2007 May. 29(5):518-27. [Medline].

  28. Zhang R, Cai JC, Zhou HW, Nasu M, Chen GX. Genotypic characterization and in vitro activities of tigecycline and polymyxin B for members of the Enterobacteriaceae with decreased susceptibility to carbapenems. J Med Microbiol. 2011 Dec. 60:1813-9. [Medline].

  29. Jacoby GA. AmpC beta-lactamases. Clin Microbiol Rev. 2009 Jan. 22(1):161-82, Table of Contents. [Medline]. [Full Text].

  30. Heller I, Grif K, Orth D. Emergence of VIM-1-carbapenemase-producing Enterobacter cloacae in Tyrol, Austria. J Med Microbiol. 2012 Apr. 61:567-71. [Medline].

  31. Deshpande P, Rodrigues C, Shetty A, Kapadia F, Hedge A, Soman R. New Delhi Metallo-beta lactamase (NDM-1) in Enterobacteriaceae: treatment options with carbapenems compromised. J Assoc Physicians India. 2010 Mar. 58:147-9. [Medline].

  32. Lowman W, Sriruttan C, Nana T, et al. NDM-1 has arrived: first report of a carbapenem resistance mechanism in South Africa. S Afr Med J. 2011 Nov 25. 101(12):873-5. [Medline].

  33. Bush K, Jacoby GA, Medeiros AA. A functional classification scheme for beta-lactamases and its correlation with molecular structure. Antimicrob Agents Chemother. 1995 Jun. 39(6):1211-33. [Medline].

  34. Woodford N, Dallow JW, Hill RL, et al. Ertapenem resistance among Klebsiella and Enterobacter submitted in the UK to a reference laboratory. Int J Antimicrob Agents. 2007 Apr. 29(4):456-9. [Medline].

  35. Souli M, Kontopidou FV, Papadomichelakis E, et al. Clinical experience of serious infections caused by Enterobacteriaceae producing VIM-1 metallo-beta-lactamase in a Greek University Hospital. Clin Infect Dis. 2008 Mar 15. 46(6):847-54. [Medline].

  36. Pintado V, San Miguel LG, Grill F, et al. Intravenous colistin sulphomethate sodium for therapy of infections due to multidrug-resistant gram-negative bacteria. J Infect. 2008 Mar. 56(3):185-90. [Medline].

  37. Gupta S, Govil D, Kakar PN, Prakash O, Arora D, Das S. Colistin and polymyxin B: A re-emergence. Indian J Crit Care Med. 2009 Apr-Jun. 13(2):49-53. [Medline]. [Full Text].

  38. Lo-Ten-Foe JR, de Smet AM, Diederen BM, et al. Comparative evaluation of the VITEK 2, disk diffusion, etest, broth microdilution, and agar dilution susceptibility testing methods for colistin in clinical isolates, including heteroresistant Enterobacter cloacae and Acinetobacter baumannii strains. Antimicrob Agents Chemother. 2007 Oct. 51(10):3726-30. [Medline].

  39. Gales AC, Jones RN, Sader HS. Global assessment of the antimicrobial activity of polymyxin B against 54 731 clinical isolates of Gram-negative bacilli: report from the SENTRY antimicrobial surveillance programme (2001-2004). Clin Microbiol Infect. 2006 Apr. 12(4):315-21. [Medline].

  40. Walkty A, DeCorby M, Nichol K, Karlowsky JA, Hoban DJ, Zhanel GG. In vitro activity of colistin (polymyxin E) against 3,480 isolates of gram-negative bacilli obtained from patients in Canadian hospitals in the CANWARD study, 2007-2008. Antimicrob Agents Chemother. 2009 Nov. 53(11):4924-6. [Medline]. [Full Text].

  41. Hawser SP, Bouchillon SK, Hoban DJ, Badal RE. In vitro susceptibilities of aerobic and facultative anaerobic Gram-negative bacilli from patients with intra-abdominal infections worldwide from 2005-2007: results from the SMART study. Int J Antimicrob Agents. 2009 Dec. 34(6):585-8. [Medline].

  42. Bassetti M, Righi E, Fasce R, et al. Efficacy of ertapenem in the treatment of early ventilator-associated pneumonia caused by extended-spectrum beta-lactamase-producing organisms in an intensive care unit. J Antimicrob Chemother. 2007 Aug. 60(2):433-5. [Medline].

  43. Yang FC, Yan JJ, Hung KH, Wu JJ. Characterization of ertapenem-resistant Enterobacter cloacae in a Taiwanese university hospital. J Clin Microbiol. 2012 Feb. 50(2):223-6. [Medline]. [Full Text].

  44. Abbott SL, Janda JM. Enterobacter cancerogenus ("Enterobacter taylorae") infections associated with severe trauma or crush injuries. Am J Clin Pathol. 1997 Mar. 107(3):359-61. [Medline].

  45. Alhambra A, Cuadros JA, Cacho J, et al. In vitro susceptibility of recent antibiotic-resistant urinary pathogens to ertapenem and 12 other antibiotics. J Antimicrob Chemother. 2004 Jun. 53(6):1090-4. [Medline].

  46. Caplan ES, Hoyt NJ. Identification and treatment of infections in multiply traumatized patients. Am J Med. 1985 Jul 15. 79(1A):68-76. [Medline].

  47. Clark NM, Patterson J, Lynch JP 3rd. Antimicrobial resistance among gram-negative organisms in the intensive care unit. Curr Opin Crit Care. 2003 Oct. 9(5):413-23. [Medline].

  48. Cosgrove SE, Kaye KS, Eliopoulous GM, et al. Health and economic outcomes of the emergence of third-generation cephalosporin resistance in Enterobacter species. Arch Intern Med. 2002 Jan 28. 162(2):185-90. [Medline].

  49. Cunha BA. Antibiotic Essentials. 9th ed. Sudbury, MA: Jones & Bartlett; 2010.

  50. Cunha BA. Enterobacter: Colonization & infection. Infect Dis Pract. 1999. 23:41-3.

  51. Cunha BA. Once-daily tigecycline therapy of multidrug-resistant and non-multidrug-resistant gram-negative bacteremias. J Chemother. 2007 Apr. 19(2):232-3. [Medline].

  52. Cunha BA. Pharmacokinetic considerations regarding tigecycline for multidrug-resistant (MDR) Klebsiella pneumoniae or MDR Acinetobacter baumannii urosepsis. J Clin Microbiol. 2009 May. 47(5):1613. [Medline]. [Full Text].

  53. Cunha BA, McDermott B, Nausheen S. Single daily high-dose tigecycline therapy of a multidrug-resistant (MDR) Klebsiella pneumoniae and Enterobacter aerogenes nosocomial urinary tract infection. J Chemother. 2007 Dec. 19(6):753-4. [Medline].

  54. Cunha BA, Theodoris AC, Yannelli B. Enterobacter cloacae graft infection/bacteremia in a hemodialysis patient. Am J Infect Control. 2000 Apr. 28(2):181-3. [Medline].

  55. De Champs C, Sirot D, Chanal C, et al. A 1998 survey of extended-spectrum beta-lactamases in Enterobacteriaceae in France. The French Study Group. Antimicrob Agents Chemother. 2000 Nov. 44(11):3177-9. [Medline].

  56. Donati L, Scamazzo F, Gervasoni M, et al. Infection and antibiotic therapy in 4000 burned patients treated in Milan, Italy, between 1976 and 1988. Burns. 1993 Aug. 19(4):345-8. [Medline].

  57. Foster DR, Rhoney DH. Enterobacter meningitis: organism susceptibilities, antimicrobial therapy and related outcomes. Surg Neurol. 2005 Jun. 63(6):533-7; discussion 537. [Medline].

  58. Fritsche TR, Stilwell MG, Jones RN. Antimicrobial activity of doripenem (S-4661): a global surveillance report (2003). Clin Microbiol Infect. 2005 Dec. 11(12):974-84. [Medline].

  59. Fritsche TR, Strabala PA, Sader HS, et al. Activity of tigecycline tested against a global collection of Enterobacteriaceae, including tetracycline-resistant isolates. Diagn Microbiol Infect Dis. 2005 Jul. 52(3):209-13. [Medline].

  60. Gallagher PG. Enterobacter bacteremia in pediatric patients. Rev Infect Dis. 1990 Sep-Oct. 12(5):808-12. [Medline].

  61. Hanna H, Afif C, Alakech B, Boktour M, et al. Central venous catheter-related bacteremia due to gram-negative bacilli: significance of catheter removal in preventing relapse. Infect Control Hosp Epidemiol. 2004 Aug. 25(8):646-9. [Medline].

  62. Hoffmann H, Sturenburg E, Heesemann J, et al. Prevalence of extended-spectrum beta-lactamases in isolates of the Enterobacter cloacae complex from German hospitals. Clin Microbiol Infect. 2006 Apr. 12(4):322-30. [Medline].

  63. Jiang X, Ni Y, Jiang Y, et al. Outbreak of infection caused by Enterobacter cloacae producing the novel VEB-3 beta-lactamase in China. J Clin Microbiol. 2005 Feb. 43(2):826-31. [Medline].

  64. Kang CI, Kim SH, Park WB, et al. Bloodstream infections caused by Enterobacter species: predictors of 30-day mortality rate and impact of broad-spectrum cephalosporin resistance on outcome. Clin Infect Dis. 2004 Sep 15. 39(6):812-8. [Medline].

  65. Kaye KS, Cosgrove S, Harris A, et al. Risk factors for emergence of resistance to broad-spectrum cephalosporins among Enterobacter spp. Antimicrob Agents Chemother. 2001 Sep. 45(9):2628-30. [Medline].

  66. Larson EL, Cimiotti JP, Haas J, et al. Gram-negative bacilli associated with catheter-associated and non-catheter-associated bloodstream infections and hand carriage by healthcare workers in neonatal intensive care units. Pediatr Crit Care Med. 2005 Jul. 6(4):457-61. [Medline].

  67. Leverstein-van Hall MA, Blok HE, et al. Extensive hospital-wide spread of a multidrug-resistant enterobacter cloacae clone, with late detection due to a variable antibiogram and frequent patient transfer. J Clin Microbiol. 2006 Feb. 44(2):518-24. [Medline].

  68. Liu CP, Wang NY, Lee CM, et al. Nosocomial and community-acquired Enterobacter cloacae bloodstream infection: risk factors for and prevalence of SHV-12 in multiresistant isolates in a medical centre. J Hosp Infect. 2004 Sep. 58(1):63-77. [Medline].

  69. Livermore DM. beta-Lactamases in laboratory and clinical resistance. Clin Microbiol Rev. 1995 Oct. 8(4):557-84. [Medline].

  70. Livermore DM, Oakton KJ, Carter MW, et al. Activity of ertapenem (MK-0826) versus Enterobacteriaceae with potent beta-lactamases. Antimicrob Agents Chemother. 2001 Oct. 45(10):2831-7. [Medline].

  71. Luzzaro F, Docquier JD, Colinon C, et al. Emergence in Klebsiella pneumoniae and Enterobacter cloacae clinical isolates of the VIM-4 metallo-beta-lactamase encoded by a conjugative plasmid. Antimicrob Agents Chemother. 2004 Feb. 48(2):648-50. [Medline].

  72. Markowitz SM, Smith SM, Williams DS. Retrospective analysis of plasmid patterns in a study of burn unit outbreaks of infection due to Enterobacter cloacae. J Infect Dis. 1983 Jul. 148(1):18-23. [Medline].

  73. Mushtaq S, Ge Y, Livermore DM. Comparative activities of doripenem versus isolates, mutants, and transconjugants of Enterobacteriaceae and Acinetobacter spp. with characterized beta-lactamases. Antimicrob Agents Chemother. 2004 Apr. 48(4):1313-9. [Medline].

  74. Paterson DL, Rossi F, Baquero F, et al. In vitro susceptibilities of aerobic and facultative Gram-negative bacilli isolated from patients with intra-abdominal infections worldwide: the 2003 Study for Monitoring Antimicrobial Resistance Trends (SMART). J Antimicrob Chemother. 2005 Jun. 55(6):965-73. [Medline].

  75. Pitout JD, Nordmann P, Laupland KB, et al. Emergence of Enterobacteriaceae producing extended-spectrum beta-lactamases (ESBLs) in the community. J Antimicrob Chemother. 2005 Jul. 56(1):52-9. [Medline].

  76. Pitout JD, Thomson KS, Hanson ND, et al. Plasmid-mediated resistance to expanded-spectrum cephalosporins among Enterobacter aerogenes strains. Antimicrob Agents Chemother. 1998 Mar. 42(3):596-600. [Medline].

  77. Ristuccia PA, Cunha BA. Enterobacter. Infect Control. 1985 Mar. 6(3):124-8. [Medline].

  78. Rupp ME, Fey PD. Extended spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae: considerations for diagnosis, prevention and drug treatment. Drugs. 2003. 63(4):353-65. [Medline].

  79. Sader HS, Jones RN, Dowzicky MJ, et al. Antimicrobial activity of tigecycline tested against nosocomial bacterial pathogens from patients hospitalized in the intensive care unit. Diagn Microbiol Infect Dis. 2005 Jul. 52(3):203-8. [Medline].

  80. Sader HS, Jones RN, Stilwell MG, et al. Tigecycline activity tested against 26,474 bloodstream infection isolates: a collection from 6 continents. Diagn Microbiol Infect Dis. 2005 Jul. 52(3):181-6. [Medline].

  81. Sanders CC, Sanders WE Jr. beta-Lactam resistance in gram-negative bacteria: global trends and clinical impact. Clin Infect Dis. 1992 Nov. 15(5):824-39. [Medline].

  82. Sanders WE Jr, Sanders CC. Enterobacter spp.: pathogens poised to flourish at the turn of the century. Clin Microbiol Rev. 1997 Apr. 10(2):220-41. [Medline].

  83. Siegel JD, Rhinehart E, Jackson M, Chiarello L and the HICPAC. Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare SEttings 2007. Centers for Disease Contol. Available at http://www.cdc.gov/ncidod/dhqp/pdf/guidelines/Isolation2007.pdf. Accessed: 1 April 12008.

  84. Siegel JD, Rhinehart E, Jackson M, Chiarello L, HICPAC. Management of Multidrug-Resistant Organisms In Healthcare Settings, 2006. Centers for Disease Control. Available at http://www.cdc.gov/ncidod/dhqp/pdf/ar/mdroGuideline2006.pdf. Accessed: accessed 1 April 2008.

  85. Tresoldi AT, Padoveze MC, Trabasso P, et al. Enterobacter cloacae sepsis outbreak in a newborn unit caused by contaminated total parenteral nutrition solution. Am J Infect Control. 2000 Jun. 28(3):258-61. [Medline].

  86. v Dijk Y, Bik EM, Hochstenbach-Vernooij S, v d Vlist GJ, Savelkoul PH, Kaan JA, et al. Management of an outbreak of Enterobacter cloacae in a neonatal unit using simple preventive measures. J Hosp Infect. 2002 May. 51(1):21-6. [Medline].

  87. Watson JT, Jones RC, Siston AM, et al. Outbreak of catheter-associated Klebsiella oxytoca and Enterobacter cloacae bloodstream infections in an oncology chemotherapy center. Arch Intern Med. 2005 Dec 12-26. 165(22):2639-43. [Medline].

  88. Wendt C, Lin D, von Baum H. Risk factors for colonization with third-generation cephalosporin-resistant enterobacteriaceae. Infection. 2005 Oct. 33(5-6):327-32. [Medline].

  89. Wisplinghoff H, Bischoff T, Tallent SM, et al. Nosocomial bloodstream infections in US hospitals: analysis of 24,179 cases from a prospective nationwide surveillance study. Clin Infect Dis. 2004 Aug 1. 39(3):309-17. [Medline].

  90. Lazarovitch T, Amity K, Coyle JR, Ackerman B, Tal-Jasper R, Ofer-Friedman H, et al. The Complex Epidemiology of Carbapenem-Resistant Enterobacter Infections: A Multicenter Descriptive Analysis. Infect Control Hosp Epidemiol. 2015 Sep 24. 1-9. [Medline].

 
Previous
Next
 
Radiograph of an open right tibial fracture in a 21-year-old male marine who was wounded when an improvised explosive device detonated while he was on patrol in Iraq.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.